Feeding by the tobacco specialist Manduca sexta (Lepidoptera, Sphingidae) and application of larval oral secretions and regurgitant (R) to mechanical wounds are known to elicit: (a) a systemic release of mono-and sesquiterpenes, (b) a jasmonate burst, and (c) R-specific changes in transcript accumulation of putatively growth-and defense-related mRNAs in Nicotiana attenuata Torr. ex Wats. We identified several fatty acid-amino acid conjugates (FACs) in the R of M. sexta and the closely related species Manduca quinquemaculata which, when synthesized and applied to mechanical wounds at concentrations comparable with those found in R, elicited all three R-specific responses. Ion-exchange treatment of R, which removed all detectable FACs and free fatty acids (FAs), also removed all detectable activity. The biological activity of ion-exchanged R could be completely restored by the addition of synthetic FACs at R-equivalent concentrations, whereas the addition of FAs did not restore the biological activity of R. We conclude that the biological activity of R is not related to the supply of FAs to the octadecanoid cascade for endogenous jasmonate biosynthesis, but that FACs elicit the herbivore-specific responses by another mechanism and that the insect-produced modification of plant-derived FAs is necessary for the plant's recognition of this specialized herbivore.
Herbivore attack elicits costly defenses that are known to decrease plant fitness by using resources that are normally slated for growth and reproduction. Additionally, plants have evolved mechanisms for tolerating attack, which are not understood on a molecular level. Using 11 C-photosynthate labeling as well as sugar and enzyme measurements, we found rapid changes in sink-source relations in the annual Nicotiana attenuata after simulated herbivore attacks, which increased the allocation of sugars to roots. This herbivore-induced response is regulated by the -subunit of an SnRK1 (SNF1-related kinase) protein kinase, GAL83, transcripts of which are rapidly down-regulated in source leaves after herbivore attack and, when silenced, increase assimilate transport to roots. This C diversion response is activated by herbivore-specific elicitors and is independent of jasmonate signaling, which regulates most of the plant's defense responses. Herbivore attack during early stages of development increases root reserves, which, in turn, delays senescence and prolongs flowering. That attacked GAL83-silenced plants use their enhanced root reserves to prolong reproduction demonstrates that SnRK1 alters resource allocation so that plants better tolerate herbivory. This tolerance mechanism complements the likely defensive value of diverting resources to a less vulnerable location within the plant.carbon-11 ͉ defense ͉ plant-herbivore interactions ͉ tolerance P lants have evolved a variety of mechanisms for reducing the negative impact of herbivore attack on fitness; these mechanisms include direct and indirect defenses and tolerance (1). Defenses are costly, expending energy and resources that could otherwise be used to grow and generate offspring. Inducible defenses allow plants to invest resources into defense only when needed. Although defenses limit the extent of damage, even well defended plants lose large amounts of tissue when attacked by herbivores that have adapted to their defenses. Then, plants would benefit from tolerance, which minimizes the fitness consequences of tissue loss to herbivores (2-4). Defense against, and tolerance of, herbivory are not mutually exclusive; most plantinsect interactions likely combine both (5, 6). In contrast to the rapid advances in our understanding of defense mechanisms, little is known about the traits that allow plants to tolerate herbivore damage.Tolerance, which is measured by comparing the fitness of a genotype in environments with and without attackers, remains uncharacterized at the molecular level (2, 7). At a physiological level, increases in photosynthetic rate, branching, and storage in belowground tissues are thought to be involved (8-10). These responses require the tuning of primary metabolism, for which mutant screens and other reverse genetic approaches with model plants have yet to yield molecular regulators. Host plants that have coevolved with adapted herbivores likely have elaborate defense and tolerance responses to minimize the fitness consequences of herbivory...
Plants respond to herbivore attack with a dramatic functional reorganization that involves the activation of direct and indirect defenses and tolerance, which in turn make large demands on primary metabolism. Here we provide the first characterization of the transcriptional reorganization that occurs after insect attack in a model plant-herbivore system: Nicotiana attenuata Torr. ex Wats.-Manduca sexta. We used mRNA differential display to characterize one-twentieth of the insect-responsive transcriptome of N. attenuata and verified differential expression for 27 cDNAs. Northern analyses were used to study the effects of folivory and exposure to airborne methyl jasmonate and for kinetic analyses throughout a 16-hlight/8-h-dark cycle. Sequence similarity searches allowed putative functions to be assigned to 15 transcripts. Genes were related to photosynthesis, electron transport, cytoskeleton, carbon and nitrogen metabolism, signaling, and a group responding to stress, wounding, or invasion of pathogens. Overall, transcripts involved in photosynthesis were strongly down-regulated, whereas those responding to stress, wounding, and pathogens and involved in shifting carbon and nitrogen to defense were strongly up-regulated. The majority of transcripts responded similarly to airborne methyl jasmonate and folivory, and had tissue-and diurnal-specific patterns of expression. Transcripts encoding Thr deaminase (TD) and a putative retrotransposon were absent in control plants, but were strongly induced after herbivory. Full-length sequences were obtained for TD and the pathogen-inducible ␣-dioxygenase, PIOX. Effects of abiotic and biotic stimuli were investigated for transcripts encoding TD, importin ␣, PIOX, and a GAL83-like kinase cofactor.
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